1. IMMUNOLOGY IN PARASITIC INFECTIONS YL6 ASMPH WINIFREDA U. DE LEON

2. PARASITES UNICELLULAR - PROTOZOA MALARIA AMEBIASIS TRYPANOSOMIASIS MULTICELLULAR – HELMINTHS SCHISTOSOMIASIS FILARIASIS HOOKWORM DSE STRONGYLOIDOSIS

3. WHY INFECTED INDIVIDUALS RESPOND DIFFERENTLY TO THE SAME PARASITE?

4. HOST- PARASITE INTERACTION HOST – WANTS TO PROTECT HIMSELF FROM THE PARASITE PARASITE – WANTS TO EVADE HUMAN DEFENSES

5. HOST FACTORS GENETICS – GENERAL MAKE-UP MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) HUMAN LEUCOCYTE ANTIGEN (HLA) e.g. SICKLE CELL TRAIT – PROTECTS VS PLAS FALCIPARUM MALARIA DUFFY BLOOD FACTOR – SUSCEPTIBLE TO PLAS VIVAX MALARIA NUTRITIONAL STATUS HIGH PROTEIN – NOT GOOD FOR INTESTINAL PROTOZOAN HIGH CARBOHYDRATE – GOOD FOR TAPEWORMS LOW IRON – RISK FOR DEVELOPMENT OF ANEMIA HORMONAL BALANCE AGE

6. NON-SPECIFIC DEFENSES HOST PHYSICAL AND CHEMICAL BARRIER SKIN SPHINCTERS SECRETIONS/ EXCRETIONS MEMBERS OF NORMAL FLORA ACID pH : gastric vagina HUMAN REFLEXES

7. SKIN LAYERS

8. INTACT SKIN PARASITE HOST HOOKWORMS FILARIFORM STRONGYLOIDES FILARIFORM HYALURONIDASE – AIDS IN SKIN PENETRATION SCHISTOSOMA CERCARIAE PENETRATION GLANDS

9. ACIDIC pH HOST VAGINAL CANAL TRICHOMONAS VAGINALIS - AFFECTED GASTRO INTESTINAL TRACT ENTAMEBA HISTOLYTICA CYST GIARDIA LAMBLIA CYST ASCARIS EGG ) TRICHURIS EGG ) THICK EGG SHELL TAENIA EGGS )

10. MUCUS MEMBRANE

12. MUCUS SECRETION HOST CAN ENVELOP PARASITE – MOTILITY OF GIARDIA LAMBLIA TROPHOZOITES W/C CAN DIMINISH PATHOLOGY

13. HUMAN REFLEXES COUGHING EXPULSION OF LUNG FLUKE EGGS EXPULSION OF ADULT ASCARIS URINATION FLUSH OUT TRICHOMONAS VAGINALIS

14. INFLAMMATORY RESPONSES PHAGOCYTES COMPLEMENT HUMORAL MEDIATORS BRADYKININS FIBRINOLYTIC SYSTEMS

16. PHAGOCYTES

17. CELLULAR COMPONENTS EOSINOPHILS/ NEUTROPHILS INCREASE IN NUMBER EXHIBIT KILLING ACTION MACROPHAGES PHAGOCYTOSIS

18. NEUTROPHIL EXTRA- CELLULAR TRAPS

19. LYMPHOID COMPONENTS SKIN ASSOCIATED LYMPHOID TISSUES (SALT) LANGERHANS CELLS DENDRITIC CELLS MAST CELLS GUT ASSOCIATED LYMPHOID TISSUES (GALT)

20. LYMPH NODES

21. HOST STATUS OUTCOME IMMUNOCOMPETENT - RESISTANCE IMMUNE-COMPROMISED SUSCEPTIBILITY PATHOLOGY

22. INFECTION PATIENT - EXPOSURE TO PARASITE ANTIGEN ACQUIRED IMMUNE DEFENSE -RECOGNITION OF NON SELF -HAS MEMORY -SPECIFIC

23. PURPOSE DISTINGUISHES SELF FROM NONSELF ELIMINATES THE NON SELF

24. SPECIFIC/ ADAPTIVE DEFENSES IMMUNE RESPONSES HUMORAL B- LYMPHOCYTES AND ANTIBODIES CELL MEDIATED T-LYMPHOCYTES AND THEIR SOLUBLE PRODUCTS

25. ANTIGEN MAY BE PRESENT ONLY IN ONE STAGE OF PARASITE DEVELOPMENT OR MAY BE PRESENT IN ALL STAGES ANTIGEN ANTIGEN PRESENTING CELLS T- HELPER LYMPHOCYTES

26. SUBSETS TH1 Th2 INTERLEUKIN 2 ILN 4,5 & 6 GAMMA INTERFERON CYTOTOXIC LYMPHOCYTES B- LYMPHOCYTES CMIR PLASMA CELLS (ANTIBODIES) HIR

28. CLASSES OF IMMUNOGLOBULINS

29. ANTIBODIES IMMUNOGLOBULINS IgE, IgG, IgM AND IgA NON SPECIFIC + HIR + CMIR CAN WORK AT THE SAME TIME IgE + MAST CELLS, EOSINOPHILS & GOBLET CELLS = EXPULSION OF GIT HELMINTHS IgE + INFLAMMATORY CELLS = CYTOCIDAL ACTION ON SCHISTOSOMA spp

30. ANTIBODY DEPENDENT CELL MEDIATED CYTOTOXICITY (ADDC) IgE + EOSINOPHILS EOSINOPHIL ACTIVATING FACTOR INTERLEUKIN 5 GRANULOCYTE –MONOCYTE COLONY STIMULATING FACTOR DESTRUCTION OF MICROFILARIAE SCHISTOSOME

31. ADCC

32. ANAPHYLAXIS IgE + HOMOCYTOTROPHIC IgG1 = DEGRANULATION OF MAST CELLS AND BASOPHILS = TYPE 1 HYPERSENSITIVITY HYDATID CYST ARTHROPOD BITES

33. MAST CELL DEGRANULATION

34. HYDATID CYST ECHINOCOCCUS GRANULOSUS

35. IgM AND IgG NOT EFFECTIVE AGAINST GIT HELMINTHS OPSONIZATION (PHAGOCYTOSIS) OF TRYPANOSOMES PREVENT PENETRATION OF HOST CELLS: RBC (PLASMODIA, BABESIA) IgM AND IgG + COMPLEMENT = LYSIS OF TRYPANOSOMES

36. IgA IgA + IgM = MEDIATE ADCC IN GIARDIA INFECTION IgA + IgG + CMI = SEPARATION OF CRYPTOSPORIDIUM FROM ENTEROCYTES IgA + GALT = PROTECTIVE vs INTESTINAL HELMINTHS (TAPEWORM)

37. MACROPHAGES ANTIGEN PRESENTING CELLS PRODUCED BY LYMPHOKINE ACTIVATION : INTRACELLULAR DESTRUCTION -OF PLASMODIUM/ BABESIA IN RBC -OF LEISHMANIA IN MACROPHAGES

39. T LYMPHOCYTES Th (HELPER) – ANTIBODY PRODUCTION Tdth (DELAYED TYPE OF HYPERSENSITIVITY) – PRODUCTION OF LYMPHOKINES - RECRUITMENT OF CELLS INTO GRANULOMA FORMATION e.g. SCHISTOSOMA Tc (CYTOTOXIC)- CANNOT KILL HELMINTHS BUT CAN DESTROY PARASITIZED CELLS Ts (SUPPRESSOR) + MACROPHAGES = REGULATION/ MODULATION OF IMMUNE RESPONSE

40. Th1 RESPONSE Th1 + GAMMA INTERFERON MINIMIZES ILN 13 CAN PROTECT vs FIBROSIS IN SCHISTOSOMA INFECTION

41. PARASITE EVASION MECHANISMS vs HOST PARASITE GLYCAN IMMUNE SUPPRESSION ANTIGENIC VARIATION HOST MIMICRY SEQUESTRATION

42. PARASITE GLYCAN

43. IMMUNE SUPPRESSION PLASMODIA – REDUCES THE IMMUNE FUNCTION OF MACROPHAGES - LESSEN PHAGOCYTOSIS - DEFECTIVE PROCESSING OF ANTIGEN AFRICAN TRYPANOSOMES – PRODUCTION OF LARGE AMOUNT OF VARIABLE SURFACE GLYCOPROTEINS (VSG’s) - DEFECTIVE ANTIGEN PROCESSING - IMPAIR T & B CELL ACTIVITIES

44. HOOKWORM ADULTS IN THE INTESTINES Produces glycoprotein ( Neutrophil inhibitory factor (NIF) that can resist acute inflammatory response 1. Blocks the adhesion of activated human neutrophils to vascular endothelial cells 2. Blocks the release of H2O2 from activated neutrophils 3. Blocks the ingestion of serum opsonized particles by inhibiting neutrophil binding to the integrin receptor CD11, CD13 and CD18

46. HOOKWORM ADULTS Excretory-Secretory Products - Stimulates fibrinolysis Glutathione S transferase Anti IgG enzyme Acetylcholinesterase Prevents expulsion of the parasite

47. IMMUNE SUPPRESSION ENTAMEBA HISTOLYTICA SUPPRESSOR FACTOR vs MONOCYTES FASCIOLA spp – DOWN REGULATION OF Th1 ACTIVITY FILARIAL WORMS/ PLASMODIA POLYCLONAL HYPER- GAMMA GLOBULINEMIA NO SPECIFICITY

48. IMMUNE SUPPRESSION BLOCKING ANTIBODIES FILARIAL WORMS HOOKWORM (NECATOR) IMMUNE RESPONSE OF MAN IS DIRECTED TO DEEP LAYERS OF THE HOOKWORM CUTICLE

49. IMMUNE SUPPRESSION IMMUNE COMPLEXES PLASMODIUM spp TRYPANOSOMA CRUZI CYSTICERCUS CELLULOSAE SCHISTOSOMA SUPPRESS INFLAMMATORY REACTION THROUGH INHIBITION OF COMPLEMENT NO DESTRUCTION OF PARASITE

50. ANTIGENIC VARIATION CHANGE IN ANTIGENIC PROFILE TRYPANOSOMA GAMBIENSE GIARDIA LAMBLIA VARIATION IN THE AMINO ACID SEQUENCE IN PLASMODIUM FALCIPARUM MEROZOITE SURFACE ANTIGEN (MSA) RING INFECTED ERYTHROCYTE SURFACE ANTIGEN (RESA)

51. TRYPANOSOMA GAMBIENSE

52. Pf VARIATION

54. P. FALCIPARUM – GENETIC REGULATION

56. HOST MIMICRY MIMICS ANTIGEN OF HOST ECHINOCOCCUS GRANULOSUS BLOOD GROUP ANTIGEN ACQUIRES ANTIGENIC MOLECULES OF HOST SCHISTOSOMA spp

57. SEQUESTRATION ESCAPE THE HOST IMMUNE RESPONSE HIDE INSIDE MACROPHAGES TRYPANOSOMA CRUZI LEISHMANIA spp TOXOPLASMA GONDII HIDE IN THE DEEP VASCULATURE PLAS FALCIPARUM (KNOBS FOR ATTACHMENT TO TINY CAPILLARIES

58. PARASITES – EVADE PHAGOCYTOSIS

59. CEREBRAL MALARIA

60. ARE THESE IMMUNE RESPONSES PROTECTIVE ? FILARIASIS TROPICAL PULMONARY EOSINOPHILIA HYPERGAMMAGLOBULINEMIA OVER PRODUCTION OF IgM DEVELOPMENT OF IMMUNE COMPLEXES

61. TPE

62. IMMUNE COMPLEXES MALARIA (PLASMODIUM) HYPERACTIVE MALARIUS SPLEEN (HMS) DISTURBANCE IN HIR SPLENOMEGALY AND ANEMIA PLAS MALARIAE – DEPOSITED IN GLOMERULI CAUSING KIDNEY FAILURE/ NEPHROTIC SYNDROME

63. IMMUNE COMPLEXES

64. OTHER ADVERSE EFFECTS SEQUESTRATION PLAS FALCIPARUM CAUSES CEREBRAL INVOLVEMENT LEISHMANIA DESTRUCTION OF MACROPHAGES GRANULOMA FORMATION SCHISTOSOMA MAIN CAUSE OF PATHOLOGY

65. OTHER ADVERSE EFFECTS LOSS OF HIR IMMUNE-DEFICIENCY AT RISK OF OPPORTUNISTIC PARASITIC INFECTIONS LOSS OF CMIR STRONGYLOIDOSIS TRIGGERS EXTRAINTESTINAL DISSEMINATION

66. AREAS OF INTEREST IMMUNOREGULATION CHRONIC INFECTION – DAMPENS T- CELL RESPONSIVENESS EFFECT OF NITRIC OXIDES + ILN 10 ON PATHOLOGY

67. AREAS OF INTEREST INTERACTION BETWEEN ENDOCRINE SYSTEM AND IL 6 PREMUNITION OR CONCOMITANT IMMUNITY IMMUNE RESPONSE TO CO- INFECTION POSSIBILITY OF IMMUNOLOGICAL DISORDER LIKE AUTO-IMMUNITY

68. HOW TO APPLY IN MEDICAL SCIENCE IMMUNODIAGNOSIS Ab DETECTION Ag DETECTION VACCINE DEVELOPMENT DRUG DEVELOPMENT

69. ANTIBODY DETECTION

70. THANK YOU AND GOOD DAY